Clinical Attachment Loss Classification Essay

Abstract

The Diagnosis and classification of periodontal diseases has remained a dilemma since long. Two distinct concepts have been used to define diseases: Essentialism and Nominalism. Essentialistic concept implies the real existence of disease whereas; nominalistic concept states that the names of diseases are the convenient way of stating concisely the endpoint of a diagnostic process. It generally advances from assessment of symptoms and signs toward knowledge of causation and gives a feasible option to name the disease for which etiology is either unknown or it is too complex to access in routine clinical practice. Various classifications have been proposed by the American Academy of Periodontology (AAP) in 1986, 1989 and 1999. The AAP 1999 classification is among the most widely used classification. But this classification also has demerits which provide impediment for its use in day to day practice. Hence a classification and diagnostic system is required which can help the clinician to access the patient's need and provide a suitable treatment which is in harmony with the diagnosis for that particular case. Here is an attempt to propose a practicable classification and diagnostic system of periodontal diseases for better treatment outcome.

Keywords: Classification, periodontal disease, practicable classification

INTRODUCTION

Historically, Periodontal Diseases were named based upon the cluster of symptoms. As the clinical descriptions became more sophisticated, there started classification of diseases into separate groups, and from this came new insight into disease etiology.[1] Various forms of periodontal and mucogingival diseases have been diagnosed and discussed in the past with varying explanations.

Two distinct concepts have been used to define diseases: Essentialism and Nominalism. The essentialistic concept implies the real existence of a disease. But the concept is deceptive for quite a few fine reasons, like many diseases remain of unknown origin and if the origin is known it could either be of diverse type or complex type with the interplay of several factors, e.g. Aggressive periodontitis is the interplay of genetic and systemic factors. Nominalism, the counterpart of essentialism implies that a disease name is just a name given to a group of subjects who share a group of well-defined signs and symptoms. Ideally, a nominalistic disease definition describes a set of criteria that is fulfilled by all the persons said to have the disease, but not fulfilled by the person that are considered free from the disease.[2] Scadding et al. supported the nominalistic concept and stated that the name of diseases are a convenient way of stating concisely the endpoint of a diagnostic process that advances from assessment of symptoms and signs towards the knowledge of causation.

Naming the periodontal disease on the basis of essentialistic concept is intricate because of the fact that the periodontal diseases are of multiple origin caused due to interplay of complex genetic, local, systemic and environmental factors. Microbiologic factors have been proposed to be associated with different periodontal conditions, but studies are still needed to answer many questions like why same bacteria causes destruction at one site and no or minimum destruction at the other site. So it is difficult to diagnose periodontal diseases on the etiological basis. It is evident that diagnosing various conditions and classifying them on the basis of sound knowledge is of prime importance, merely assembling the facts is insufficient. But the present knowledge of the periodontal disease seems insufficient to satisfactorily explain the terminology used to define different periodontal conditions.[3]

The purpose of the diagnosis is screening of the disease in an asymptomatic individual, classify a disease category, treatment planning, monitoring of treatment efficacy and disease recurrence.[4] However, the design of the previous classifications and diagnostic system is such that it creates a state of dilemma in which either chief complaint, goal of the therapy, diagnosis or treatment plan is overlooked or ignored. Generally, the diagnosis is made in response to the overall status of the periodontium and treatment is planned accordingly without considering the patient's complaint and goal of the therapy.

The Purpose of the present classification is to build a diagnostic system that is in harmony with the goal of the periodontal therapy with special emphasis on:

  1. Eliminating the unknown and complex factors from the classification which are either complex or difficult to access in day to day practice.

  2. Develop a harmonious relationship between chief complaint, diagnosis, treatment plan and goal of the therapy.

  3. To avoid over exaggerated examination, which in turn decreases the trauma to inflamed periodontal tissue during initial periodontal therapy.

Origin of classification systems and their demerits

Fauchard in 1723 coined the term “Scurvy” that was for the periodontal diseases of the gums.[5] Gottlieb for the first time in 1920 classified the periodontal diseases into 4 groups Schmutz-pyorrhoae, alveolar atrophy or diffuse atrophy, paradental-pyorrhoae and occlusal trauma.[6] Schmutz-pyorrhoae is somewhat similar to the present day mild periodontitis characterized by shallow pockets and abundant local factors. Paradental-pyorrhoae depicts moderate to severe periodontitis consisting of irregular distribution of deep to moderate pockets. Alveolar atrophy comes closer to present day aggressive periodontitis and occlusal trauma is somewhat similar to present day's “trauma from occlusion” (TFO).

McCall and Box introduced the term “periodontitis” to inflammatory diseases in which all three components of the Periodontium, i.e. The gingiva, bone, and periodontal ligament were affected.[7] Orban and Weinmann coined term “periodontosis” to designate non-inflammatory disease.[8] “Periodontosis” was considered as a separate disease entity, distinctly different from periodontitis, which was considered as a sequel of gingivitis of the deeper periodontal structures, and therefore, of inflammatory origin. Butler introduced the name “Juvenile Periodontitis” instead of “periodontosis” when describing the periodontal condition of young individuals with severe periodontal bone loss.[9]

Page and Schroeder divided periodontal diseases into Pre-pubertal, Juvenile, Rapidly progressive, Adult periodontitis and Acute necrotizing ulcerative gingivo-periodontitis (ANUG/P).[10] It is important to note that with the exception of ANUG/P, the age of onset was of decisive importance. This notion was adopted in almost all subsequent classifications; moreover, there were no definite criteria behind dividing the disease except the age limitation.

American Academy of Periodontology (AAP) 1986 classification, classified periodontal diseases into juvenile periodontitis, pre-pubertal, local juvenile, generalized juvenile, adult periodontitis, ANUG/P and refractory periodontitis.[11] This classification also followed same criteria to divide them according to age limits but was complicated by adding the pre-pubertal under the juvenile periodontitis category.

AAP 1989 classification added a new category of periodontitis associated with systemic diseases and organized the early onset periodontitis into pre-pubertal, juvenile and rapidly progressing.[12] However, the author haven’t given any consistent basis for classification except for the age criteria used in the previous classification. Other disadvantages of this classification included extensive overlap between the different diagnostic categories. The quality of treatment provided previously and the patient response to therapy was required.

The first European Workshop 1993 accepted the fact that there is insufficient knowledge to separate truly different diseases (disease heterogeneity) from differences in the presentation/severity of the same disease (phenotypic variation) and stated that the existing classifications are unsatisfactory.[13] The 1993 classification proposed a simple classification distinguishing between 1. Early onset periodontitis, 2. Adult periodontitis, 3. Necrotizing periodontitis. However, there was a need to use additional secondary descriptors for defining the clinical situation. These include: Distribution within the dentition, rate of progression, response to treatment, relation to systemic diseases, microbiological, ethnic group characteristics, and other factors. But the change in the classification system has still not solved the purpose behind as there was considerable uncertainty about arbitrarily setting an upper age limit for patients with so-called early onset periodontitis. e.g., what if 21 year male has typical incisor molar pattern, so the age was of decisive importance. Further the rate of progression in the past and response to the therapy was also required for secondary description.

AAP 1999 classification, proposed a new classification and was widely accepted for many reasons such as an improvement with regard to the category of gingival diseases.[14] Adult periodontitis was renamed as “chronic periodontitis” on the basis of speculation that slowly progressive disease could be present at any age, i.e. in adults as well as in adolescents. There was the elimination of separate disease category for “refractory periodontitis.” The elucidation of the designation “periodontitis as a manifestation of systemic disease” was given. A list of diseases which are commonly manifested in the oral cavity was given. There was the addition of new categories like abscess, endodontic-periodontic lesion, development and acquired deformity which were not explained in the previous classifications. But this classification also falls short to answer many issues. The term “chronic” and “aggressive” periodontitis arose the need for the rate of progression of the disease and how much severe disease could be categorized as “aggressive periodontitis.” Primary criteria given by Lang for aggressive periodontitis need a detailed systemic investigation, familial history and rate of progression, which are difficult to access in clinical practices.

Further, the studies related to the rate of disease progression seem to be insufficient. There are many questions, which remain unanswered like why Diabetes mellitus has not been given place for the systemic condition modifying the periodontal disease. There is no description about environmental factors affecting the periodontitis and gingivitis, when there are so many proven studies available for them, e.g., smoking. Moreover, the entities like “color of gingiva” and “gingival enlargements” are included in periodontal disease category. There is no description about what degree of increase in size of gingiva could be designated as gingival enlargement?

In case of multiple diagnoses, as is the case most of the times, which diagnosis is to be put first? Patient may not come with the complaint which actually requires the treatment before the present complaint, so a disparity develop between the chief complain, diagnosis and treatment plan. Further there are situations, where the etiology of a disease is unknown; in those conditions the relation between diagnosis and the treatment plan creates a state of perplexity.

After the review of the previous classifications, it can be concluded that none of the classification comes near to the idealistic classification. AAP 1999 classification is the most widely accepted classification and used for most of research and academic purposes. Vander valden 2005 classification made an attempt to simplify the terminology but failed to reach the realistic goal, the classification still deals with same problems, which were existing in the previous classification systems. Armitage comment,[3] “The present knowledge of the periodontal disease seems to be insufficient to classify them on the basis of host/infection paradigm” still stands true. Despite of latest advancements in the research, our treatment modalities are based on the conventional concepts, so sometimes a state of confusion arises between the patient's chief complaint, diagnosis and the treatment plan.

Development of new classification system

It is of utmost importance to understand that for a successful treatment, there should be a harmonious relationship between the patient's chief complaint, diagnosis, goal of therapy and treatment plan. Goal of therapy should be realistic; an overenthusiastic goal is bound to be a failure.

Concept of primary and secondary diagnosis

Diagnosis is the basic foundation for the treatment plan. However, the present classification gives a long list of periodontal diseases, which is difficult to apply in day to day practice. A state of confusion arises when there are multiple diagnosis for a case as which one to be put first? There are situations when etiology of the complaint remains obscure, in those cases a disharmony develops between diagnosis and treatment. e.g., A patient come with a complain of pain in upper right first molar, but the clinician does not find any relevant cause for the pain, in those cases most times the diagnosis is based on the overall status of periodontal tissue rather than the complaint of the patient and hence a disparity develops between the complaint of the patient and treatment plan. So the concept of primary and secondary diagnosis comes into the picture.

Primary diagnosis

It is a diagnosis made in response to the patient's chief complaint to justify patient's immediate complaint and suggests the treatment plan to achieve the immediate goal of the therapy [Figure 1].

Figure 1

Sequence of Periodontal Treatment

Secondary diagnosis

It is a diagnosis which reveals the patients actual periodontal health status irrespective of patient's chief complaint and suggests a treatment plan to achieve the ultimate, ideal or pragmatic goal.

It is important to note here that both the primary and secondary diagnosis can be same, when the patient's chief complaint reflects the overall status of the oral cavity. There can be more than one diagnosis in each category. There may not be any primary diagnosis if patients complaint is vague or if the main etiology is obscure, in that case secondary diagnosis will be the only diagnosis but cannot be called as the primary diagnosis.

Depending upon the goal of the therapy either of the diagnosis can be used and fulfilled.

Goals of the periodontal therapy

The goal of treatment should be pre decided based on the patient's expectation and prognosis for the case.

Immediate goal

The immediate goal of therapy is to prevent, arrest, control, or eliminate the periodontal disease.

Ideal goal: The ideal goal aims to promote healing through regeneration of the lost form, function, esthetics, and comfort.

Pragmatic goal: When the ideal goal cannot be achieved, the pragmatic goal of therapy would be to repair the damage resulting from the disease.

Ultimate goal: Finally, the ultimate goal of therapy is to sustain the masticatory apparatus-especially teeth, or their analogues, in the state of health.[15]

How to start clinical examination

Assessment of gingival status

A gingival examination should begin with the assessment of the gingival inflammation. The Color of the gingiva, edema, suppuration and bleeding on probing (BOP) are the parameters which help in the assessment of the gingival inflammation. Color of the gingiva has the least positive predictive value and BOP has the highest positive predictive value.[16]

Assessment of periodontal status

Periodontal destruction should be assessed by probing depth, clinical attachment loss (CAL) and radiographs. BOP can be used as a parameter to access the activity or inactivity of the disease. Finding the etiology should be a secondary requisite which can be achieved by mean of microbial culture, biochemical methods and immunological assays.

At this stage, probing depth is inaccurate because the measurements are recorded on the inflamed tissue. The Accurate scores can be obtained only after the reduction of inflammation. So probing should be done grossly, to assess the periodontal attachment loss or in contrary radiographs can be used. Measurement of the CAL at this level should not be tried.

Presence of any abscess or sinus opening, carious lesion, wasting disease, root stumps and mobility should be accessed. Radiological investigation: Intraoral periapical (IOPA) and Orthopantogram OPG (if required) and routine blood investigation: Clotting time, bleeding time, hemoglobin percentage and blood sugar etc. should be carried out as and when needed.

After scaling and root planning: (base line examination) measurement of recession, mobility (re-evaluate), CAL, Pocket depth, and Edema should be performed. There may be a need for the reassessment of radiological, hematological and microbiological test. At this stage, one should make secondary diagnosis and treatment plan accordingly.

List of diagnosis

Gingival diseases

Gingival diseases are mostly chronic and generalized in nature so rather than calling them as chronic gingivitis the term plaque induced gingival disease is more appropriate as it describes the nature of the disease as well. Further, if the conditions which modify the gingival disease [Table 1] are also present, they have to be mentioned in the diagnosis. Gingival conditions, which are not primarily induced by plaque or are a manifestation of the systemic conditions should be put in the category of non-plaque induced gingival disease [Table 2]. In this way, gingival conditions can be put under either of the under mentioned categories

Table 1

Systemic conditions affecting the gingivitis

Table 2

Non-plaque induced gingival destruction

  1. Plaque induced gingival disease.

  2. Plaque induced gingival disease modified by systemic factors.

  3. Non-plaque induced gingival disease

Periodontal diseases

The disease under the term “chronic periodontitis” is put under the category of “Plaque induced periodontal destruction” with secondary description [Table 3] to explain extent, pattern and other characteristics. Severity of the periodontal disease can be divided into mild (bone loss less than 1/3rd of the root surface), moderate (bone loss more than 1/3rd and less than 2/3rd of the root surface), sever (bone loss more than 2/3rd of the root surface). Extent of the disease can be incidental (1 tooth affected), localized (2-7 teeth affected), generalized (More than 7 teeth affected) The periods of activity/inactivity of the periodontal diseases should be accessed on the basis of signs of inflammation. CAL over a period of time should be used as a parameter to monitor the periodontal tissue stability in the maintenance phase.[17]

Table 3

Secondary description for periodontal disease

Systemic diseases and conditions like diabetes mellitus, bruxism/environmental factors like smoking, stress affecting periodontal destruction, if present have to be mentioned in a separate category “Plaque induced periodontal destruction influenced by systemic disease/condition/environmental factor.” A separate disease category should be assigned for the disease causing periodontal destruction irrespective of the presence or absence of plaque. Such disease should be put under the category of periodontal destruction as a manifestation of systemic disease [Table 4]. In most of the older classifications recession is considered as a finding rather than diagnosis. But we consider recession as a separate entity with a definite line of treatment. Further two variants of recession can be separated based on the etiology, one which is due to inflammation and starts at the Interdental area and the other one which starts on the facial and lingual surface due to tooth brush trauma. Post-scaling sensitivity, which is a common phenomenon and renders the patient to move from one dentist to other, such a problem should be put under a category “Iatrogenic cemental tear” although the term Iatrogenic mimic as if there is a part of dentist in it but from the past evidences it is clear that some amount of cemental tear is always associated with scaling and root planning and hence justify the terminology. Halitosis is a very common problem with varying etiology, so a list of factors associated with halitosis is mentioned [Table 5]. So the diagnosis of halitosis can be written as follows: Halitosis associated with suppurative periodontitis, halitosis associated with tooth related factors, halitosis associated with diabetes, halitosis of Idiopathic factors. Periodontal destruction due to ongoing orthodontic treatment or faulty prosthesis/endodontic treatment comes under a category named as “compromised periodontium of iatrogenic origin.”

Table 4

Systemic factors manifested in the oral cavity

None of the previous classification has discussed about implant related problems. This classification provides a simple yet effective classification for implant related problems also. The problems related to implant can be divided into 3 categories: “Ailing implant,” which has soft tissue problems around the implant without any marked mobility/loss of function. “Failing implant,” which has the increasing mobility over a period of time, but implant being still in function. “Failed implant” is that, having a marked mobility and loss of function.

  • Etiology and diagnosis of the aggressive periodontitis is complex and provide diagnostic problems in clinical setup, moreover, there are cases which neither set in the category of chronic periodontitis nor in aggressive periodontitis, so a special category of “periodontal disease of complex idiopathic factors” is introduced, where patients are having periodontal disease of undiagnosed syndrome/familial/genetic/immunological/systemic variation. Necrotizing periodontal disease. Disease categories such as abscesses of periodontium, periodontal disease associated with endodontic lesions, mucogingival, acquired or developmental disorders, TFO kept same as in AAP 1999 classification.

In this way, periodontal diseases can be put under either of the under mentioned categories.

  • Plaque induced periodontal destruction

  • Plaque induced periodontal destruction influenced by systemic disease/condition/environmental factor.

  • Periodontal destruction as a manifestation of systemic disease.

  • Necrotizing periodontal disease.

  • Abscesses of Periodontium.

  • Periodontal disease associated with endodontic lesions

  • Recession

    • a)

      Inflammatory (which begins in the Interdental area)

    • b)

      Non-inflammatory (from tooth brush trauma, mostly facial surface is affected).

  • Mucogingival problem (inadequate width/volume of attached gingiva, aberrant frenum, shallow vestibule and gingival color).

  • Iatrogenic cemental tear

  • Acquired or developmental disorders.

  • TFO: Primary TFO

    Secondary TFO

  • Compromised Periodontium of iatrogenic origin (due to orthodontic therapy).

  • Halitosis (secondary description).

  • Implant related problems: Ailing implant, Failing implant, Failed implant

  • Endodontic or prosthodontic need with respective area.

  • Periodontal disease of complex idiopathic factors.

Footnotes

Source of Support: Nil

Conflict of Interest: None declared.

REFERENCES

1. Temple LK, McLeod RS, Gallinger S, Wright JG. Essays on science and society. Defining disease in the genomics era. Science. 2001;293:807–8.[PubMed]

2. Wulff HR, Gotzsche PC. Evidence-based Clinical Decision Making. 3rd ed. Oxford: Blackwell Science; 2000. The disease classification. Rational Diagnosis and Treatment; pp. 39–62.

3. van der Velden U. Purpose and problems of periodontal disease classification. Periodontol 2000. 2005;39:13–21.[PubMed]

4. Mombelli A. Critical issues in periodontal diagnosis. Periodontol 2000. 2005;39:9–12.[PubMed]

5. Gold SI. Periodontics. The past. Part (I). Early sources. J Clin Periodontol. 1985;12:79–97.[PubMed]

6. Gottlieb B. The formation of the pocket: Diffuse atrophy of alveolar bone. J Am Dent Assoc. 1928;15:462–76.

7. McCall JO, Box HK. The pathology and diagnosis of the basic lesions of chronic periodontitis. J Am Dent Assoc. 1925;12:1300–9.

8. Orban B, Weinmann JP. Diffuse atrophy of the alveolar bone. J Periodontol. 1942;13:31–45.

9. Butler JH. A familial pattern of juvenile periodontitis (periodontosis) J Periodontol. 1969;40:115–8.[PubMed]

10. Page RC, Schroeder HE. Basel: Karger; 1982. Periodontitis in Man and Other Animals. A Comparative Review.

11. Chicago: The American Academy of Periodontology; 1989. The American Academy of Periodontology. Proceedings of the World Workshop in Clinical Periodontics; pp. I/23–4.

12. Princeton NJ. Periodontal diagnosis and diagnostic aids. Proceedings of the world workshop in clinical periodontics. Consensus report, discussion section I. Am Acad Periodontol. 1989;2:13–20.

13. Tonetti MS. Etiology and pathogenesis. In: Lang NP, Karring T, editors. Proceedings of the 1st European Workshop on Periodontology. Chicago: Quintessence Books; 1994. pp. 54–89.

14. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol. 1999;4:1–6.[PubMed]

15. Consensus Report Discussion Section 11, Proceedings of the World Workshop in Clinical Periodontics. 1989;11:13–20.

16. Armitage GC. Periodontal diseases: Diagnosis. J Periodontol Ann. 1996;1:37–215.[PubMed]

17. American Academy of Periodontology. Parameter on aggressive periodontitis. J Periodontol. 2000;71:767–9.[PubMed]

Schizophrenia Revision Notes


by Bruce Johnson published 2017


Exam Advice

You MUST revise everything - because the exam board could choose any question, however, it does make sense to spend more time on those topics which have not appeared for a while.

Exam Tip:

With these particular questions there is a sizeable risk that people don’t understand the difference between the questions, and then write about the wrong thing. Make sure you know which is which, for example do you understand the difference between “genetic explanation” and “neural correlates explanation”, and do you have a model essay for each?


Section 1: Diagnosis and Classification of Schizophrenia

Psychologists use the DSM and ICD to diagnose a patient with schizophrenia.

In order to diagnose Schizophrenia the Mental Health Profession developed the DSM (Diagnostic and Statistical Manual) still used today as a method of classifying mental disorders (particularly in the USA). It is also used as a basis for the ICD (International Classification of Diseases) used by the World Health Organisation in classifying all disorders (mental and physical).

Note: you may come across the terms DSM-IV and ICD-10. These refer to the latest editions of the two classification systems.

Positive Symptoms - an excess or distortion of normal functions: including hallucinations and delusions

Positive symptoms are an excess or distortion of normal functions, for example hallucinations, delusions and thought disturbances such as thought insertion.

AO1

• Hallucinations are usually auditory or visual perceptions of things that are not present. Imagined stimuli could involve any of the senses. Voices are usually heard coming from outside the person’s head giving instructions on how to behave.

• Delusions are false beliefs. Usually the person has convinced him/herself that he/she is someone powerful or important, such as Jesus Christ, the Queen (e.g. Delusions of Grandeur). There are also delusions of being paranoid, worrying that people are out to get them.

• Psychomotor Disturbances: Stereotypyical - Rocking backwards and forwards, twitches, & repetitive behaviors. Catatonia- staying in position for hours/days on end, cut off from the world.

Negative Symptoms – where normal functions are limited: including speech poverty and avolition.

Negative symptoms are a diminution or loss of normal functions such as psychomotor disturbances, lack of volition, disturbances of mood and thought disorders.

AO1

• Thought disorder in which there are breaks in the train of thought and the person appears to make illogical jumps from one topic to another (loose association). Words may become confused and sentences incoherent (so called ‘word salad). Broadcasting is a thought disorder whereby a person believes their thoughts are being broadcast to others, for example over the radio or through TV. Alogia - aka speech poverty – is a thought disorder were correct words are used but with little meaning.

• Avolition: Lack of volition (i.e. desire): in which a person becomes totally apathetic and sits around waiting for things to happen. They engage in no self motivated behavior. Their get up and go has got up and gone!

Classification AO3

Slater & Roth (1969) say that hallucinations are the least important of all the symptoms, as they are not exclusive to schizophrenic people.

Classification and diagnosis does have advantages as it allows doctors to communicate more effectively about a patient and use similar terminology when discussing them. In addition, they can then predict the outcome of the disorder and suggest related treatment to help the patient.

Scheff (1966) points out that diagnosis classification labels the individual, and this can have many adverse effects, such as a self-fulfilling prophecy (patients may begin to act how they are expected to act), and lower self-esteem.

Ethics – do the benefits of classification (care, treatment, safety) outweigh the costs (possible misdiagnosis, mistreatment, loss of rights and responsibility, prejudice due to labelling).

Reliability and Validity in Diagnosis and Classification of Schizophrenia with reference to co-morbidity, culture and gender bias and symptom overlap.

Reliability - AO1

For the classification system to be reliable, differfent clinicians using the same system (e.g. DSM) should arrive at the same diagnosis for the same individual.

AO3

Diagnosis of schizophrenia is difficult as the practitioner has no physical signs but only symptoms (what the patient reports) to make a decision on.

Jakobsen et al. (2005) tested the reliability of the ICD-10 classification system in diagnosing schizophrenia. A hundred Danish patients with a history of psychosis were assessed using operational criteria, and a concordance rate of 98% was obtained. This demonstrates the high reliability of the clinical diagnosis of schizophrenia using up-to-date classification.

Comorbidity describes people who suffer from two or more mental disorders. For example, schizophrenia and depression are often found together. This makes it more difficult to confidently diagnose schizophrenia. Comorbidity occurs because the symptoms of different disorders overlap. For example, major depression and schizophrenia both involve very low levels of motivation. This creates problems of reliability. Does the low motivation reflect depression or schizophrenia, or both?

Gender bias: Loring and Powell (1988) found that some behavior which was regarded as psychotic in males was not regarded as psychotic in females.

Validity - AO1

For the classification system to be valid it should be meaningful and classify a real pattern of symptoms, which result from a real underlying cause.

AO3

The validity of schizophrenia as a single disorder is questioned by many. This is a useful point to emphasise in any essay on the disorder. There is no such thing as a ‘normal’ schizophrenic exhibiting the usual symptoms.

Since their are problems with the validity of diagnois classification, unsuitable treatment may be administered, sometimes on an involuntary basis. This raises practical and ethical issues when selecting different types of tretment.

Problems of validity: Are we really testing what we think we are testing? In the USA only 20% of psychiatric patients were classed as having schizophrenia in the 1930s but this rose to 80% in the 1950’s . In London the rate remained at 20%, suggesting neither group had a valid definition of schizophrenia.

Neuropsychologist Michael Foster Green suggests that neurocognitive deficits in basic functions such as memory, attention, central executive and problem solving skills may combine to have an outcome which we are labelling “Schizophrenia” as if it was the cause when in fact it is simply an umbrella term for a set of effects.

Predictive validity. If diagnosis leads to successful treatment, the diagnosis can be seen as valid. But in fact some Schizophrenics are successfully treated whereas others are not. Heather (1976) there is only a 50% chance of predicting what treatment a patient will receive based on diagnosis, suggesting that diagnosis is not valid.

Aetiological validity – for a diagnosis to be valid, all patients diagnosed as schizophrenic should have the same cause for their disorder. This is not the case with schizophrenia: The causes may be one of biological or psychological or both.

David Rosenhan (1972) famous experiment involving Pseudopatients led to 8 normal people being kept in hospital despite behaving normally. This suggests the doctors had no valid method for detecting schizophrenia. They assumed the bogus patients were schizophrenic with no real evidence. In a follow up study they rejected genuine patients whom they assumed were part of the deception.

Culture - One of the biggest controversies in relation to classification and diagnosis is to do with cultural relativism and variations in diagnosis. For example in some Asian countries people are not expected to show emotional expression, whereas in certain Arabic cultures public emotion is encouraged and understood. Without this knowledge a person displaying overt emotional behavior in a Western culture might be regarded as abnormal. Cochrane (1977) reported that the incidence of schizophrenia in the West Indies and the UK is 1 %, but that people of Afro-Caribbean origin are seven times more likely to be diagnosed as schizophrenic when living in the UK,


Section 2: Biological Explanations for Schizophrenia

AO1

• Benzel et al. (2007) three genes: COMT , DRD4 , AKT1 - have all been associated with excess dopamine in specific D2 receptors, leading to acute episodes, positive symptoms which include delusions, hallucinations, strange attitudes.

• Research by Miyakawa et al. (2003) studied DNA from human families affected by schizophrenia and found that those with the disease were more likely to have a defective version of a gene, called PPP3CC which is associated with the production of calcineurin which regulates the immune system. Also, research by Sherrington et al. (1988) has found a gene located on chromosome 5 which has been linked in a small number of extended families where they have the disorder.

• Evidence suggests that the closer the biological relationship, the greater the risk of developing schizophrenia. Kendler (1985) has shown that first-degree relatives of those with schizophrenia are 18 times more at risk than the general population. Gottesman (1991) has found that schizophrenia is more common in the biological relatives of a schizophrenic, and that the closer the degree of genetic relatedness, the greater the risk.

AO3

Very important to note genetics are only partly responsible, otherwise identical twins would have 100% concordance rates.

One weakness of the genetic explanation of schizophrenia is that there are methodological problems. Family, twin and adoption studies must be considered cautiously because they are retrospective, and diagnosis may be biased by knowledge that other family members who may have been diagnosed. This suggests that there may be problems of demand characteristics.

A second weakness is the problem of nature-v-Nurture. It is very difficult to separate out the influence of nature-v-nurture. The fact that the concordance rates are not 100% means that schizophrenia cannot wholly be explained by genes and it could be that the individual has a pre-disposition to schizophrenia and simply makes the individual more at risk of developing the disorder. This suggests that the biological account cannot give a full explanation of the disorder.

A final weakness of the genetic explanation of schizophrenia is that it is biologically reductionist. The Genome Project has increased understanding of the complexity of the gene. Given that a much lower number of genes exist than anticipated, it is now recognised that genes have multiple functions and that many genes behavior. Schizophrenia is a multi-factorial trait as it is the result of multiple genes and environmental factors. This suggests that the research into gene mapping is oversimplistic as schizophrenia is not due to a single gene.

AO1

• Dopamine is a neurotransmitter. It is one of the chemicals in the brain which causes neurons to fire. The original dopamine hypothesis stated that schizophrenia suffered from an excessive amount of dopamine. This causes the neurons that use dopamine to fire too often and transmit too many messages.

• High dopamine activity leads to acute episodes, and positive symptoms which include: delusions, hallucinations, confused thinking.

• Evidence for this comes from that fact that amphetamines increase the amounts of dopamine. Large doses of amphetamine given to people with no history of psychological disorders produce behavior which is very similar to paranoid schizophrenia. Small doses given to people already suffering from schizophrenia tend to worsen their symptoms.

• A second explanation developed, which suggests that it is not excessive dopamine but that fact that there are more dopamine receptors. More receptors lead to more firing and an over production of messages. Autopsies have found that there are generally a large number of dopamine receptors (Owen et al., 1987) and there was an increase in the amount of dopamine in the left amygdale (falkai et al. 1988) and increased dopamine in the caudate nucleus and putamen (Owen et al, 1978).

AO3

One criticism of the dopamine hypothesis is there is a problem with the chicken and egg. Is the raised dopamine levels the cause of the schizophrenia, or is it the raised dopamine level the result of schizophrenia? It is not clear which comes first. This suggests that one needs to be careful when establishing cause and effect relationships in schizophrenic patients.

One of the biggest criticisms of the dopamine hypothesis came when Farde et al found no difference between schizophrenics’ levels of dopamine compared with ‘healthy’ individuals in 1990.

Noll (2009) also argues around one third of patients do not respond to drugs which block dopamine so other neurotransmitters may be involved.

A final weakness of the dopamine hypothesis is that it is biologically deterministic. The reason for this is because if the individual does have excessive amounts of dopamine then does it really mean that thy ey will develop schizophrenia? This suggests that the dopamine hypothesis does not account for freewill.

AO1

• People with schizophrenia have abnormally large ventricles in the brain. Ventricles are fluid filled cavities (i.e. holes) in the brain that supply nutrients and remove waste. This means that the brains of schizophrenics are lighter than normal. The ventricles of a person with schizophrenia are on average about 15% bigger than normal (Torrey, 2002).

AO3

A strength is that the research into enlarged ventricles and neurotransmitter levels have high reliability. The reason for this is because the research is carried out in highly controlled environments, which specialist, high tech equipment such as MRI and PET scans. These machines take accurate readings of brain regions such as the frontal and pre-frontal cortex, the basil ganglia, the hippocampus and the amygdale. This suggests that if this research was tested and re-tested the same results would be achieved.

Supporting evidence for the brain structure explanation comes from further empirical support from Suddath et al. (1990). He used MRI (magnetic resonance imaging) to obtain pictures of the brain structure of MZ twins in which one twin was schizophrenic. The schizophrenic twin generally had more enlarged ventricles and a reduced anterior hypothalamus. The differences were so large the schizophrenic twins could be easily identified from the brain images in 12 out of 15 pairs. This suggests that there is wider academic credibility for enlarged ventricles determining the likelihood of schizophrenia developing.

A second weakness of the neuroanatomical explanations is that it is biologically deterministic. The reason for this is because if the individual does have large ventricles then does it really mean that they will develop schizophrenia? This suggests that the dopamine hypothesis does not account for freewill.


Section 3: Psychological Explanations for Schizophrenia

AO1

• Laing and others rejected the medical / biological explanation of mental disorders. They did not believe that schizophrenia was a disease. They believed that schizophrenia was a result of social pressures from life. Laing believed that schizophrenia was a result of the interactions between people, especially in families.

• Bateson et al. (1956) suggested the double bind theory, which suggests that children who frequently receive contradictory messages from their parents are more likely to develop schizophrenia. For example parents who say they care whilst appearing critical or who express love whilst appearing angry. They did not believe that schizophrenia was a disease. They believed that schizophrenia was a result of social pressures from life.

• Prolonged exposure to such interactions prevents the development of an internally coherent construction of reality; in the long run, this manifests itself as typically schizophrenic symptoms such as flattening affect, delusions and hallucinations, incoherent thinking and speaking, and in some cases paranoia.

• Another family variable associated with schizophrenia is a negative emotional climate, or more generally a high degree of expressed emotion (EE). EE is a family communication style that involves criticism, hostility and emotional over-involvement. The researchers concluded that this is more important in maintaining schizophrenia than in causing it in the first place, (Brown et al 1958). Schizophrenics returning to such a family were more likely to relapse into the disorder than those returning to a family low in EE. The rate of relapse was particularly high if returning to a high EE family was coupled with no medication.

AO3

One strength of the double bind explanation comes from further empirical support provided by Berger (1965). They found that schizophrenics reported a higher recall of double bind statements by their mothers than non-schizophrenics. However, evidence may not be reliable as patient’s recall may be affected by their schizophrenia. This suggests that there is wider academic credibility for the idea of contradictory messages causing schizophrenia.

A second strength of the research into expressed emotion (EE) is that it has practical applications. For example Hogarty (1991) produced a type of therapy session, which reduced social conflicts between parents and their children which reduced EE and thus relapse rates. This suggests that gaining an insight into family relationships allows psychiatric professionals to help improve the quality of patient’s lives.

A weakness of the family relationsships appraoch is that there is a problem of cause and effect. Mischler & Waxler (1968) found significant differences in the way mothers spoke to their schizophrenic daughters compared to their normal daughters, which suggests that dysfunctional communication may be a result of living with the schizophrenic rather than the cause of the disorder. This suggests that there is a problem of the chicken and egg scenario in relation to expressed emotion causing schizophrenia.

A second weakness of the double bind theory is that there are ethical issues. There are serious ethical concerns in blaming the family, particularly as there is little evidence upon which to base this. Gender bias is also an issue as the mother tends to be blamed the most, which means such research is highly socially sensitive. This suggests that the research therefore does not protect individuals from harm.

Cognitive explanations: including dysfunctional thought processing

Cognitive approaches examine how people think, how they process information. Researchers have focused on two factors which appear to be related to some of the experiences and behaviors of people diagnosed with schizophrenia. First, cognitive deficits which are impairments in thought processes such as perception, memory and attention. Second, cognitive biases are present when people notice, pay attention to, or remember certain types of information better than other.

AO1

Cognitive Deficits

• There is evidence that people diagnosed as schizophrenic have difficulties in processing various types of information, for example visual and auditory information. Research indicates their attention skills may be deficient – they often appear easily distracted.

• A number of researchers have suggested that difficulties in understanding other people’s behavior might explain some of the experiences of those diagnosed as schizophrenic. Social behavior depends, in part, on using other people’s actions as clues for understanding what they might be thinking. Some people who have been diagnosed as schizophrenic appear to have difficulties with this skill.

• Cognitive deficits have been suggested as possible explanations for a range of behaviors associated with schizophrenia. These include reduced levels of emotional expression, disorganised speech and delusions.

Cognitive Biases

• Cognitive biases refer to selective attention. The idea of cognitive biases has been used to explain some of the behaviors which have been traditionally regarded as ‘symptoms’ of ‘schizophrenia’.

• - Delusions: The most common delusion that people diagnosed with schizophrenia report is that others are trying to harm or kill them – delusions of persecution. Research suggests that these delusions are associated with specific biases in reasoning about and explaining social situations. Many people who experience feelings of persecution have a general tendency to assume that other people cause the things that go wrong with their lives.

AO3

A strength of the cognitive explanation is that it has practical applications. Yellowless et al. (2002) developed a machine that produced virtual hallucinations, such as hearing the television telling you to kill yourself or one person’s face morphing into another’s. The intention is to show schizophrenics that their hallucinations are not real. This suggests that understanding the effects of cognitive deficits allows psychologists to create new initiatives for schizophrenics and improve the quality of their lives.

A final strength is that it takes on board the nurture approach to the development of schizophrenia. For example, it suggests that schizophrenic behavior is the cause of environmental factors such as cognitive factors.

One weakness of the cognitive explanation is that there are problems with cause and effect. Cognitive approaches do not explain the causes of cognitive deficits – where they come from in the first place. Is it the cognitive deficits which causes the schizophrenic behavior or is the schizophrenia that causes the cognitive deficits? This suggests that there are problems with the chicken and egg problem.

A second weakness of the cognitive model is that it is reductionist. The reason for this is because the approach does not consider other factors such as genes. It could be that the problems caused by low neurotransmitters creates the cognitive deficits. This suggests that the cognitive approach is oversimplistic when consider the explanation of schizophrenia.


Section 4: Drug Therapy: typical and atypical antipsychotics

Drug therapy is a biological treatment for schizophrenia.

AO1

• First generation Antipsychotics are called “Typical Antipsychotics” Eg. Chlorpromazine and Haloperidol.

• They arrest dopamine production by blocking the D2 receptors in synapses that absorb dopamine, in the mesolimbic pathway thus reducing positive symptoms, such as auditory hallucinations.

• But they tended to block ALL types of dopamine activity, (in other parts of the brain as well) and this caused side effects and may have been harmful.

Newer drugs, called “atypical antipsychotics” attempt to target D2 dopamine activity in the limbic system but not D3 receptors in other parts of the brain.

• They also have some effect on other neurotransmitters such as serotonin. They generally have fewer side effects eg. less effect on movement Eg. Clozapine, Olazapine and Risperidone.

AO3

Since the mid-1950s antipsychotic medications have greatly improved treatment. Medications reduce positive symptoms particularly hallucinations and delusions; and usually allow the patient to function more effectively and appropriately.

Antipsychotic drugs are highly effective as they are relatively cheap to produce, easy to administer and have a positive effect on many sufferers. However they do not "cure" schizophrenia, rather they dampen symptoms down so that patients can live fairly normal lives in the community.

Kahn et al. (2008) found that antipsychotics are generally effective for at least one year, but second- generation drugs were no more effective than first-generation ones.

Some sufferers only take a course of antipsychotics once, while others have to take a regular dose in order to prevent symptoms reappearing. There is a sizeable minority who do not respond to drug treatment. Pills are not as helpful with other symptoms, especially emotional problems. Older antipsychotics like haloperidol or chlorpromazine may produce side effects Sometimes when people with schizophrenia become depressed, so it is common to prescribe anti-depressants at the same time as the anti-psychotics.

All patients are in danger of relapsing but without medication the relapses are more common and more severe which suggests the drugs are effective.

Clozapine targets multiple neurotransmitters, not just dopamine, and has been shown to be more effective than other antipsychotics, although the possibility of severe side effects – in particular, loss of the white blood cells that fight infection Even newer antipsychotic drugs, such as risperidone and olanzapine are safer, and they also may be better tolerated. They may or may not treat the illness as well as clozapine, however.

Meta – Analysis by Crossley Et Al (2010) suggested that Atypical antipsychotics are no more effective, but do have less side effects.

Exam Tip

In most cases the original “typical antipsychotics” have more side effects, so if the exam paper asks for two biological therapies you can write about typical anti-psychotics and emphasise the side effects, then you can write about the atypical antipsychotics and give them credit for having less side effects.


Section 5: Psychological Therapies for Schizophrenia

Family Therapy is also referred to as Psychoeducation and was developed by Anderson in 1980 to counter the problem of high Expressed Emotion in families.

Aims of Family Therapy

• To educate relatives about schizophrenia.

• To stabilize the social authority of the doctor and the family.

• To improve how the family communicated and handled the situation.

• To teach patients and carers more effective stress management techniques.

Methods used in Family Therapy

• Families taught to have weekly family meetings solving problems on family and individual goals, resolve conflict between members, and pinpoint stressors.

• • Preliminary analysis: Through interviews and observation the therapist identifies strengths and weaknesses of family members and identifies problem behaviors.

• Information transfer – teaching the patient and the family the actual facts about the illness, it’s causes, the influence of drug abuse, and the effect of stress and guilt.

• Communication skills training – teach family to listen, to express emotions and to discuss things. • Additional communication skills are taught, such as “compromise and negotiation,” and “requesting a time out” . This is mainly aimed at lowering expressed emotion.

AO3

A study by Anderson et al. (1991) found a relapse rate of almost 40% when patients had drugs only, compared to only 20 % when Family Therapy or Social Skills training were used and the relapse rate was less than 5% when both were used together with the medication.

Pharaoh et al. (2003) meta - analysis found family interventions help the patient to understand their illness and to live with it, developing emotional strength and coping skills, thus reducing rates of relapse

Economic Benefits: Family therapy is highly cost effective because it reduces relapse rates, so the patients are less likely to take up hospital beds and resources.

Lobban (2013) reports that other family members felt they were able to cope better thanks to family therapy. In more extreme cases the patient might be unable to cope with the pressures of having to discuss their ideas and feelings and could become stressed by the therapy, or over-fixated with the details of their illness.

AO1

• The main idea is that behavioral change can be achieved by awarding tokens for desired ac¬tions. These reinforcers are exchanged for benefits such as a film or a coffee.

• The focus of a token economy is on shaping and positively reinforcing desired behaviors and NOT on punishing undesirable behaviors. The technique alleviates negative symptoms such as poor motivation, and nurses subsequently view patients more positively, which raises staff morale and has beneficial outcomes for patients.

• It can also reduce positive symptoms by not rewarding them, but rewarding desirable behavior instead. Desirable behavior includes self-care, taking medication, work skills, and treatment participation.

AO3

Paul and Lentz (1977) Token economy led to better overall patient functioning and less behavioral disturbance, More cost effective (lower hospital costs)

Upper and Newton (1971) found that the weight gain associated with taking antipsychotics was addressed with token economy regimes. Chronic schizophrenics achieved 3lbs of weight loss a week.

McMonagle and Sultana (2000) reviewed token economy regimes over a 15-year period, finding that they did reduce negative symptoms, though it was unclear if behavioral changes were maintained beyond the treatment programme.

It is difficult to keep this treatment going once the patients are back at home in the community. Kazdin et al. Found that changes in behavior achieved through token economies do not remain when tokens are with¬drawn, suggesting that such treatments address effects of schizophrenia rather than causes. It is not a cure.

There have also been ethical concerns as such a process is seen to be dehumanising, subjecting the patient to a regime which takes away their right to make choices. In the 1950s and 60s nurses often “rewarded” patients with cigarettes. Due to the pivotal role of dopamine in schizophrenia this led to a culture of heavy smoking an nicotine addiction in psychiatric hospitals of the era.

Cognitive behavioral Therapy

AO1

Central idea: Patients problems are based on incorrect beliefs and expectations. CBT aims to identify and alter irrational thinking including regarding:

  • General beliefs.
  • Self image.
  • Beliefs about what others think.
  • Expectations of how others will act.
  • Methods of coping with problems.

In theory, when the misunderstandings have been swept away, emotional attitudes will also improve.

Assessment: The therapist encourages the patient to explain their concerns.

• describing delusions

• reflecting on relationships

• laying out what they hope to achieve through the therapy.

Engagement:

The therapist wins the trust of the patient, so they can work together. This requires honesty, patience and unconditional acceptance. The therapist needs to accept that the illusions may seem real to the patient at the time and should be dealt with accordingly.

ABC: Get the patients to understand what is really happening in their life:

A: Antecedent - what is triggering your problem ?

B: behavior – how do you react in these situations ?

C: Consequences – what impact does that have on your relationships with others?

Normalisation:

Help the patient realise it is normal to have negative thoughts in certain situations. Therefore there is no need to feel stressed or ashamed about them.

Critical Collaborative Analysis:

Carrying on a logical discussion till the patient begins to see where their ideas are going wrong and why they developed. Work out ways to recognise negative thoughts and test faulty beliefs when they arise, and then challenge and re-think them.

Developing Alternative Explanations:

Helping the patient to find logical reasons for the things which trouble them Let the patient develop their own alternatives to their previous maladaptive behavior by looking at coping strategies and alternative explanations.

Another form of CBT: Coping Strategy Enhancement (CSE)

• Tarrier (1987) used detailed interview techniques, and found that people with schizophrenia can often identify triggers to the onset of their psychotic symptoms, and then develop their own methods of coping with the distress caused. These might include things as simple as turning up the TV to drown out the voices they were hearing!

• At least 73% of his sample reported that these strategies were successful in managing their symptoms.

• CSE aims to teach individuals to develop and apply effective coping strategies which will reduce the frequency, intensity and duration of psychotic symptoms and alleviate the accompanying distress. There are two components:

1. Education and rapport training: therapist and client work together to improve the effectiveness of the client’s own coping strategies and develop new ones.

2. Symptom targeting: a specific symptom is selected for which a particular coping strategy can be devised Strategies are practised within a session and the client is helped through any problems in applying it. They are then given homework tasks to practice, and keep a record of how it worked.

AO3

CBT does seem to reduce relapses and readmissions to hospital (NICE 2014) However the fact that these people were on medication and having regular meetings with doctors would be expected to have that effect anyway.

Turkington et al. (2006) CBT is highly effective and should be used as a mainstream treatment for schizophrenia wherever possible.

Tarrier (2005) reviewed trials of CBT, finding evidence of reduced symptoms, especially positive ones, and lower relapse rates.

Addington and Addington (2005) claim that CBT is of little use in the early stages of an acute schizophrenic episode, but perhaps more useful when the patient is more calm and beginning to worry about how life will be after they recover. In other words, it doesn’t cure schizophrenia, it just helps people get over it.

Research in Hampshire, by Kingdon and Kirschen (2006) found that CBT is not suitable for all patients, especially those who are too thought disorientated or agitated, who refuse medication, or who are too paranoid to form trusting alliances with practitioners.

As there is strong evidence that relapse is related to stress and expressed emotion within the family, it seems likely that CBT should be employed alongside family therapy in order to reduce the pressures on the individual patient.


Section 6: Interactionist Approach

The Diathesis-stress Model

AO1

• Zubin and Spring suggest that a person may be born with a predisposition towards schizophrenia which is then triggered by stress in everyday life. But if they have a supportive environment and/or good coping skills the illness may not develop.

• Tienari Et. A. (2004): Adopted children from families with schizophrenia had more chance of developing the illness than children from normal families. This supports a genetic link. However, those children from families schizophrenia were less likely to develop the illness if placed in a “good” family with kind relationships, empathy, security, etc. So environment does play a part in triggering the illness.

AO3

Falloon et al (1996) stress – such as divorce or bereavement, causes the brain to be flooded with neurotransmitters which brings on the acute episode.

Brown and Birley (1968) 50% people who had an acute schizophrenic episode had experienced a major life event in 3 weeks prior.

Substance abuse: Amphetamine and Cannabis and other drugs have also been identified as triggers as they affect serotonin and glutamate levels.

Vasos (2012) Found the risk of schizophrenia was 2.37 times greater in cities than it was in the countryside, probably due to stress levels. Hickling (1999) the stress of urban living made African-Carribean immigrants in Britain 8 to 10 times more likely to experience schizophrenia. Faris and Dunham (1939) found clear pattern of correlation between inner city environments and levels of psychosis. Pederson and Mortensen (Denmark 2001) found Scandanavian villages have very LOW levels of psychosis, but 15 years of living in a city increased risk.

Fox (1990): It is more likely that factors associated with living in poorer conditions (e.g. stress) may trigger the onset of schizophrenia, rather than individuals with schizophrenia moving down in social status.

Bentall’s meta analysis (2012) shows that stress arising from abuse in childhood increases the risk of developing schizophrenia.

Toyokawa, Et. Al (2011) Suggest many aspects of urban living – ranging from life stressors to the use of drugs, can have an effect on human epigenetics. So the stressors of modern living could cause increased schizophrenia in future generations.


About the Author

Bruce Johnson is an A-level psychology teacher, and head of sixth form at Caterham High School


→A-level Home Page|Memory Revision|Social Influence Revision |Attachment Revision|Psychopathology Revision|

Was this article useful? Please help us improve by giving feedback below


→A-level Home Page|Memory Revision|Social Influence Revision |Attachment Revision|Psychopathology Revision|

0 thoughts on “Clinical Attachment Loss Classification Essay

Leave a Reply

Your email address will not be published. Required fields are marked *